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Related Concept Videos

Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Amyloid Fibrils03:03

Amyloid Fibrils

Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining, normally used to...

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Related Experiment Video

Updated: May 20, 2026

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
06:17

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

Disease modifying drugs targeting β-amyloid.

S N Ozudogru1, C F Lippa

  • 1Department of Neurology, Drexel University College of Medicine, Philadelphia, PA 19102, USA.

American Journal of Alzheimer'S Disease and Other Dementias
|July 21, 2012
PubMed
Summary

Currently, no Alzheimer's disease treatments alter its course, only offering symptomatic relief. However, emerging anti-amyloid therapies show promise for impacting disease progression.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Gerontology

Background:

  • Alzheimer's disease (AD) currently lacks disease-modifying treatments.
  • Existing FDA-approved interventions primarily manage symptoms.
  • Significant research is underway to develop therapies targeting the underlying disease course.

Purpose of the Study:

  • To review agents in clinical trials for Alzheimer's disease.
  • To focus on therapies targeting amyloid processing.
  • To assess the potential of these agents to alter disease progression.

Main Methods:

  • Review of clinical trial data for Alzheimer's disease therapeutics.
  • Analysis of agents targeting amyloid precursor protein processing.
  • Evaluation of therapeutic outcomes in relation to disease pathogenesis.

More Related Videos

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
07:18

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Related Experiment Videos

Last Updated: May 20, 2026

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
06:17

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis

Published on: May 22, 2018

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
07:18

Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia

Published on: November 9, 2018

Main Results:

  • Several anti-amyloid agents have been investigated in clinical trials.
  • Some agents have demonstrated limited efficacy or failed.
  • Other anti-amyloid therapies continue to show potential.

Conclusions:

  • Amyloid-beta peptide is strongly implicated in Alzheimer's pathogenesis.
  • Targeting amyloid processing remains a key strategy for disease modification.
  • Future anti-amyloid therapies may offer meaningful impact on Alzheimer's disease progression.